PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15135713-1 2004 This randomized, placebo-controlled trial showed that levosimendan administration causes a significant reduction of circulating proinflammatory cytokine interleukin-6 and soluble apoptosis mediators, such as soluble Fas and Fas ligand in patients with decompensated heart failure. Simendan 54-66 interleukin 6 Homo sapiens 153-166 17126656-8 2006 Levosimendan beneficially modulated neurohormonal and inflammatory status by decreasing B-type natriuretic peptide levels (p <0.05) and by altering the ratio of interleukin-6 to interleukin-10 in favor of the latter (p <0.05). Simendan 0-12 interleukin 6 Homo sapiens 164-177 17105880-6 2006 A significant decrease in NT-proBNP (p<0.01), high-sensitivity CRP (p<0.01) and plasma IL6 (p = 0.05) was also observed in the levosimendan group, whereas these markers remained unchanged in the placebo group; similar changes were observed after each drug infusion. Simendan 133-145 interleukin 6 Homo sapiens 93-96 16713737-6 2006 In the remaining 27 patients, levosimendan decreased serum IL-6 and sFAS, 24 h after the infusion (p<0.01 and p<0.05 vs baseline), an effect sustained for 7-30 d. Serum TNF-alpha and sTNF-R1 were decreased between 48 h (p<0.01 vs baseline for both) and 7 d (p<0.05 vs baseline for sTNF-R1) after infusion. Simendan 30-42 interleukin 6 Homo sapiens 59-63 16784930-7 2006 Plasma N-terminal-pro-B-type natriuretic peptide, tumor necrosis factor-alpha, and soluble Fas ligand levels were significantly decreased only in the levosimendan group (from 1,900 +/- 223 to 1,378 +/- 170 pg/ml, 13.4 +/- 1.0 to 12.3 +/- 1.2 pg/ml, and 68.2 +/- 3.7 to 59.8 +/- 3.6 pg/ml, respectively; p <0.05 for all); interleukin-6 was also borderline reduced (p = 0.051). Simendan 150-162 interleukin 6 Homo sapiens 324-337 16054474-1 2005 In this randomized, placebo-controlled study, it was found that a 24-hour levosimendan infusion improves echocardiographic markers of abnormal left ventricular diastolic function (transmitral flow patterns and mitral annulus velocities, as assessed by transthoracic pulse-wave Doppler and tissue Doppler imaging, respectively) and reduces substances of excessive neurohormonal activation (plasma B-type natriuretic peptide and interleukin-6) in patients with advanced heart failure. Simendan 74-86 interleukin 6 Homo sapiens 427-440 15921958-4 2005 Levosimendan produced a significant reduction in BNP compared to baseline, at both 48 h (744.1+/-100 vs 1136.3+/-93.7 pg/ml, p=0.04) and 5 days (446+/-119.3 vs 1136.3+/-93.7 pg/ml, p=0.03), while IL-6 values decreased after 5 days (4.8+/-1.3 vs 8.6+/-1.5 pg/ml, p=0.01). Simendan 0-12 interleukin 6 Homo sapiens 196-200 15974888-6 2005 Levosimendan-induced improvement in contractile reserve and clinical status of severe heart failure patients, seems to be related with the reduction of major pro-inflammatory cytokines (TNF-alpha, IL-6) and soluble apoptosis signaling molecules Fas/Fas Ligand. Simendan 0-12 interleukin 6 Homo sapiens 197-201 15771921-0 2005 Levosimendan reduces plasma B-type natriuretic peptide and interleukin 6, and improves central hemodynamics in severe heart failure patients. Simendan 0-12 interleukin 6 Homo sapiens 59-72 15771921-3 2005 This study investigates whether levosimendan-induced hemodynamic improvement of CHF patients is related to the respective changes of NT-proBNP and IL-6 levels. Simendan 32-44 interleukin 6 Homo sapiens 147-151 15771921-6 2005 RESULTS: NT-proBNP and IL-6 levels were significantly reduced in severe CHF patients within 72 h after the initiation of levosimendan treatment (p<0.01 and p<0.05, respectively). Simendan 121-133 interleukin 6 Homo sapiens 23-27 15771921-9 2005 CONCLUSIONS: Our results indicate that changes of NT-pro BNP and IL-6 levels may be useful biochemical markers related with the levosimendan-induced improvement in central hemodynamics and the clinical status of decompensated advanced CHF patients. Simendan 128-140 interleukin 6 Homo sapiens 65-69 21932058-2 2012 The study was tested in a fecal peritonitis-induced septic shock model, we observed that levosimendan combined with arginine vasopressin supplemented with norepinephrine therapy resulted in lower mean pulmonary artery pressure, lactate concentrations, arterial total nitrate/nitrite, and high-mobility group box 1 levels; decreased lung wet/dry ratio, and pulmonary levels of interleukin-6, total histological scores, and improved pulmonary gas exchange when compared with norepinephrine group. Simendan 89-101 interleukin 6 Homo sapiens 376-389 25273157-7 2015 Treatment with levosimendan strongly attenuated IL-1beta-induced expression of IL-6 and IL-8 in HACM as well as E-selectin and ICAM-1 in ECs. Simendan 15-27 interleukin 6 Homo sapiens 79-83